Polyhexamethyleneguanidine hydrochloride (PHMG) is an antimicrobial biocide of the guanidine family. In the period from August 2006 to May 2007, more than 12500 patients were admitted to hospital with a history of drinking illegal cheap "vodka" in 44 different regions in Russia, of whom 9.4% died. In reality, the "vodka" was an antiseptic liquid composed of ethanol (˜93%), diethyl phthalate, and 0.1-0.14% PHMG (brand name "Extrasept-1").
We performed an analysis of the clinical features and outcome in four poisoning treatment centers in the cities of Perm, Ekaterinburg, Irkutsk, and Khabarovsk. A total of 579 patients (215 females and 364 males) with similar symptoms were included.
The main symptoms on admission included jaundice (99.7%), skin itch (78.4%), weakness (96%), anorexia (65.8%), dizziness (65.3%), nausea (54.8%), vomiting (22.6%), stomach ache (52.7%), diarrhea (32%), and fever (50%). Mild symptoms were found in 2.5% of cases, moderate in 63%, and severe in 34.5%. Laboratory results were (mean ± SD): total bilirubin 249 ± 158 µmol/L, direct bilirubin 166 ± 97 µmol/L, cholesterol 14 ± 8 mmol/L, alanine aminotransferase 207 ± 174 IU/L, aspartate aminotransferase 174 ± 230 IU/L, alkaline phosphatase 742 ± 751 IU/L, and gamma-glutamyltranspeptidase 1199 ± 1095 IU/L. Patients generally recovered over a period of 1-5 months, although high levels of alkaline phosphatase and gamma-glutamyltranspeptidase were still found in all patients examined after 6 months. Sixty-one patients (10.5%) died between 23 and 150 days after poisoning. Local cholestasis, inflammatory infiltration, and fibrosis developing into cirrhosis were found by liver biopsy.
Acute liver injury caused by PHMG-hydrochloride or PHMG in combination with either ethanol or diethyl phthalate can be characterized as cholestatic hepatitis with a severe inflammatory component causing high mortality.
Reports on adverse reactions to nitrofurantoin today are common in Sweden and constitute 10 to 12 percent of all incoming reports. We present an analysis of 921 reports of adverse reactions received by the Swedish Adverse Drug Reaction Committee during the period 1966--1976. The two largest groups consist of reports of acute pulmonary reactions (43 percent) and allergic reactions (42 percent). The remaining reports fall into any of four smaller groups, chronic pulmonary reactions, liver damage, blood dyscrasias or neuropathy. Acute pulmonary and acute allergic reactions in all aspects are very similar and carry the characteristics of an acute hypersensitivity reaction. The increasing number of reports--even in relation to sales figures--would be best explained by a continuous sensitization. Chronic pulmonary reactions (interstitial pneumonitis) afflict older patients, often after prolonged treatment with relatively small doses. We suggest that these reactions are elicited by a toxic mechanism. Seventy-one percent of all reactions were severe enough to cause the patient's hospitalization; only 1 percent was fatal. The risk of an adverse reaction varies with sex and age, increases with age and is higher in women than in men. The time has come for a re-evaluation of nitrofurantoin and its role in the treatment of urinary tract infections.
We studied age at diagnosis and disease progression of cystic fibrosis (CF) patients with a new study design, using data of 119 patients extracted from Stockholm CF Centre registry. Risk factors for overall morbidity and for lung, liver and nutritional morbidity were investigated separately using time to event methodology (Kaplan-Meier curves, proportional hazards regression). The patients were followed from: (i) healthy at diagnosis to morbidity, (ii) diagnosis with symptoms of morbidity to being free of morbidity, and (iii) free of morbidity to relapse of morbidity. Median age at diagnosis was 5.0 months. Of the patients with overall morbidity at diagnosis 50% became free of morbidity after 4.8 years; however, the patients above the age of 24 months at diagnosis had a reduced chance of becoming free of morbidity (crude hazard ratio 0.14 [95 % confidence interval 0.04, 0.45]) compared with those with diagnosis between the ages of 2 and 12 months (P
BACKGROUND: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. METHODS: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. RESULTS: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2-1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9-4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8-10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3-2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6-2.2). CONCLUSIONS: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking.
To assess the alcohol drinking patterns in a cohort of primary sclerosing cholangitis (PSC) patients and the possible influence on the development of fibrosis.
Ninety-six patients with PSC were evaluated with a validated questionnaire about a patient's lifetime drinking habits: the lifetime drinking history (LDH) questionnaire. In addition, clinical status, transient elastography and biochemistry values were analysed and registered. Patients were defined as having either significant or non-significant fibrosis. Significant fibrosis was defined as either an elastography value of = 17.3 kPa or the presence of clinical signs of cirrhosis. Patients were divided into two groups depending on their alcohol consumption patterns; no/low alcohol consumption (one drink or unit/d) and moderate/high alcohol consumption (= 1 drink or unit/d). LDH data were calculated to estimate lifetime alcohol intake (LAI), current alcohol intake, drinks per year before and after diagnosis of PSC. We also calculated the number of episodes of binge-drinking (defined as consuming = 5 drinks per occasion) in total, before and after the diagnosis of PSC.
The mean LAI was 3882 units of alcohol, giving a mean intake after onset of alcohol consumption of 2.6 units per week. Only 9% of patients consumed alcohol equal to or more than one unit per day. Current alcohol intake in patients with significant fibrosis (n = 26) was less than in patients without significant fibrosis (n = 70), as shown by lower values of phosphatidylethanol (B-PEth) (0.1 ?mol/L vs 0.33 ?mol/L, respectively, P = 0.002) and carbohydrate-deficient transferrin (CDT) (0.88% vs 1.06%, respectively, P = 0.02). Self-reported LAI was similar between the two groups. Patients with significant fibrosis reduced their alcohol intake after diagnosis from 103 to 88 units per year whereas patients without fibrosis increased their alcohol intake after PSC diagnosis from 111 to 151 units/year. There were no correlations between elastography values and intake of alcohol (units/year) (r = -0.036).
PSC patients have low alcohol consumption. The lack of correlation between fibrosis and alcohol intake indicates that a low alcohol intake is safe in these patients.
The aim of this study was to determine the risk of developing primary liver cancer in patients with a diagnosis of alcoholism, liver cirrhosis, or both. Three population-based, mutually exclusive cohorts were defined on the basis of hospital discharge diagnosis between 1965 and 1983. Complete follow-up through 1984--excluding the first year of follow-up--showed that among 8,517 patients with a diagnosis of alcoholism, 13 cancers occurred, vs. 4.2 expected (standardized incidence ratio (SIR) = 3.1; 95% confidence interval (CI) = 1.6 to 5.3); among 3,589 patients with liver cirrhosis, 59 cancers occurred, vs. 1.7 expected (SIR = 35.1; 95% CI = 26.7 to 45.3), and among 836 patients with both diagnoses, 11 cancers occurred, vs. 0.3 expected (SIR = 34.3; 95% CI = 17.1 to 61.3). Thus, alcoholism alone entailed a moderately increased risk and alcoholism with liver cirrhosis did not increase the high relative risk for liver cancer more than cirrhosis alone. We conclude that alcohol intake may be a liver carcinogen only by being causally involved in the development of cirrhosis; and further, that the risk of developing liver cancer following cirrhosis in this population is similar to or higher than that after chronic hepatitis-B-virus infection in other Western countries.